Genome-wide study identifies ~600 loci associated with risk tolerance and risky behaviors

Risk tolerance—defined as the willingness to take risks, typically to obtain some reward—varies substantially across humans and has been actively studied in the behavioral and social sciences. An individual’s risk... [ view full abstract ]

Risk tolerance—defined as the willingness to take risks, typically to obtain some reward—varies substantially across humans and has been actively studied in the behavioral and social sciences. An individual’s risk tolerance may vary across domains, but survey-based measures of general risk tolerance (e.g., “Would you describe yourself as someone who takes risks?”) have been found to be good all-around predictors of risky behaviors such as portfolio allocation, smoking, and starting one’s own business. In a combined sample of more than one million individuals, we conducted genome-wide association studies (GWAS) of general risk tolerance, adventurousness, and risky behaviors in the driving, drinking, smoking, and sexual domains. We identified ~600 approximately independent genetic loci associated with at least one of our phenotypes, including 124 with general risk tolerance. We report evidence of substantial shared genetic influences across general risk tolerance and risky behaviors: 72 of the 124 general risk tolerance loci contain a lead SNP for at least one of our other GWAS, and general risk tolerance is moderately to strongly genetically correlated (|r_g| ~ 0.25 to 0.50) with a range of risky behaviors. A polygenic score of general risk tolerance explains up to 1.6% of the variation in general risk tolerance in independent datasets. The score is also predictive of a suite of real-world measures of risky behaviors in the health, financial, career, and other domains. Our bioinformatics analyses point to the role of gene expression in brain regions that have been identified by neuroscientific studies on decision-making, notably the prefrontal cortex, basal ganglia, and midbrain. Our analyses failed to find evidence for the five main biological pathways that had been previously hypothesized to influence risk tolerance—the steroid hormone cortisol, the monoamines dopamine and serotonin, and the steroid sex hormones estrogen and testosterone. Instead, our analyses implicate genes involved in glutamatergic and GABAergic neurotransmission, which were heretofore not generally believed to play a role in risk tolerance.